Abstract
Ticagrelor, a potent P2Y12 receptor inhibitor, is used widely to manage acute coronary syndrome owing to its superior efficacy in reducing cardiovascular events compared to clopidogrel. Despite its favorable safety profile, this paper reports a case of ticagrelor-induced hepatotoxicity. A 66-year-old male with a history of pituitary macroadenoma presented with elevated liver enzymes during a preoperative assessment for tumor removal. The patient was asymptomatic. Ultrasonography revealed diffusely decreased parenchymal echogenicity with prominent portal venular wall echogenicity, suggesting acute hepatopathy, while no significant findings were observed on the computed tomography image. All viral markers were negative; only the anti-nuclear antibody was positive. A biopsy was performed to discriminate autoimmune hepatitis. The specimen showed a lymphocytic infiltrate, with eosinophils and plasma cells mainly affecting the hepatic parenchyma in zone 3. The liver enzyme levels improved when the anti platelet drugs for biopsy were discontinued, but they worsened again after the biopsy. Hence, ticagrelor, an anti-platelet agent, was suspected as the causative drug. Ticagrelor was discontinued, and the subsequent liver enzyme levels gradually returned to normal. This case highlights the need for careful monitoring of the liver function in patients receiving ticagrelor.